00:01
Okay, let's move on to a question. The following will be
effective in homozygous familial hypercholesterolemia except,colesevelam, mipomersen, ezetimibe, and rosuvastatin. Good
for you, you chose rosuvastatin. Now this is a questionthat medical students are always getting wrong. They always
get it wrong because they assume that rosuvastatin is reallypowerful. But remember statins, are definitely going to
require aggresive normal LDL production. So let's move onto the second question. What is the mechanism of action of
Ezetimibe? Is it A, a blockage of the enzyme that producesintracellular cholesterol. Is it B, increased synthesis of
PCSK9. Is it C, increased uptake of luminal cholesterol inthe blood stream or into the blood stream. Is it D, inhibition
of intestinal cholesterol transport proteins. Or is it E,reduction of the calcium slow current. Good, you chose D. So
D, inhibition of intestinal cholesterol transport proteinsreduces the level LDL in the blood. A is incorrect because
blockage of an enzyme that produces intracellular cholesterol,that's a statin. B. Increased synthesis of PCSK9, that's
actually no drug. The PCSK9 inhibitors act as immune modulatorsor immunoglobulins that attach to PCSK9 and prevent it from
doing it's job. C is wrong. Increase uptake of luminalcholesterol into the bloodstream. That almost does'nt even
make any sense and E, reduction of the inward calcium slowcurrent is wrong. They will do that to you because sometimes
they will get you confused with a cardiac drug that sound similar.
02:06
So pay attention to the drugs that you are using. Okay, let's
go on to a question again. A 55-year old male has elevated LDLcholesterol. He was started on rosuvastatin 10mg daily. His
current medications include perindopril for hypertension,aspirin, and fenofibrate for severe hypertriglyceridemia. What
do you think the most appropriate strategy is going forward.
02:34
So what should we do? Should we stop the fenofibrate as
there is a very high likelihood of a fatal drug interaction.
02:41
Should we reduce the fenofibrate dosage as there is a
potential for a fatal drug reaction. Should we continuefenofibrate but monitor liver enzymes and follow closely. Or
use a higher dose of rosuvastatin and continue the fenofibrate.
02:59
I think that's reasonable. Continue fenofibrate but monitor
liver enzymes and follow closely. Remember that a combinationof fenofibrate and rosuvastatin has a very low risk of that
really horrible fatal interaction, possibly in the 1 in 1000000range. So to stop the medication of the severe hypertriglyceridemia
in order to start a statin is not a rational choice. It might bewhat your patient wants to do, but it's not rational because
there is not a real tangible risk other than that theoreticalrisk going forward. Monitoring and being careful is the best
way to do this. Okay that's it. I hope you enjoyed the lectureand good luck on your exams.

About the Lecture

The lecture Questions – Lipid Control by Pravin Shukle, MD is from the course Cardiovascular Pharmacology. It contains the following chapters:

Question 1: Lipid Control

Question 2: Lipid Control

Case Study 1: Lipid Control

Author of lecture Questions – Lipid Control

Pravin Shukle, MD

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